Neuroinflammation is a major culprit behind brain damage and subsequent cognitive impairment in people with Alzheimer’s disease, according to a new study.
The investigation is the first of its kind in living patients, the researchers said. And the results suggest that treatments targeting inflammation could help reverse or at least slow the accumulation of pathologic tau protein in the brain, according to Tharick Pascoal, M.D., Ph.D., of the University of Pittsburgh School of Medicine, and colleagues.
This could especially benefit people with early-stage Alzheimer’s, they said.
“Many elderly people have amyloid plaques in their brains but never progress to developing Alzheimer’s disease,” Pascoal said. “We know that amyloid accumulation on its own is not enough to cause dementia. Our results suggest that it is the interaction between neuroinflammation and amyloid pathology that unleashes tau propagation and eventually leads to wide-spread brain damage and cognitive impairment.”
Laboratory studies have provided plenty of evidence that inflammation drives the spread of damaging tau fibers in Alzheimer’s disease, but the process has never before been shown in humans, Pascoal and colleagues said. Inflammation of brain immune cells, called microglial cells, is not merely a consequence of the disease, but is a key driver of the disease’s development, they found.
Perhaps not surprisingly, this neuroinflammation was more prevalent in older people and even more pronounced in patients with mild cognitive impairments and with Alzheimer’s disease and related dementias, they noted.
Full findings were published in the journal Nature Medicine.
